For more than two centuries, arterial stenoses have been associated with sounds known as bruits that are audible using a stethoscope. Auscultation (passive listening using a stethoscope) is routinely used to qualitatively assess the loudness and pitch of bruits and murmurs in many vascular diseases, such as renovascular hypertension, coronary artery disease, peripheral artery disease and internal bleeding.
It has now been established that vascular sounds associated with stenoses, aneurysms, arteriovenous fistulae and pseudoaneurysms are produced by the forces exerted on vessel walls by eddies produced when blood flows from a high-pressure region to a low-pressure region through a narrow orifice. The luminal area is reduced by a stenosis; therefore the flow velocity in the throat of the stenosis is increased. This local increase in the flow velocity creates a post-stenotic jet, if the post-stenotic expanse region is not sufficiently streamlined to prevent flow separation (i.e., the stenosis is not a “venturi tube”). Regions of high fluid shear are produced due to the difference in velocity across the boundary of the jet. These shear forces produce eddies in the flow. The presence of eddies cause fluctuations in the flow velocity and pressure in the post-stenotic region, which cause a corresponding motion in the vessel walls. The energy produced by the pressure drop across the stenosis is therefore dissipated through these mechanical vibrations of the vessel wall as well as minor viscous heating of the blood due to turbulent shear fluctuations. The local vibrations in the vessel wall and surrounding tissue manifest either as audible “bruits” and “murmurs” (20 Hz to 1000 Hz) or palpable “thrills” (5 Hz to 20 Hz) when they reach the skin surface. For less severe stenoses, the pressure drop across the stenosis is significant only during the high velocity phase, thus the bruit lasts only during the high velocity phase. For more severe stenoses, the high velocities can be present throughout the cardiac cycle.
The power spectrum of the vibration exhibits a frequency peak called the “break frequency” that is inversely related to the diameter of the orifice and directly related to the local flow velocity through the Strouhal number. Phonoangiography and phonocardiography were developed to quantify the amplitude and duration of bruits and murmurs recorded with a sensitive microphone, and quantitative carotid phonoangiography has been successfully used to measure the spectral content of the bruit signal and estimate the degree of carotid artery stenosis in multiple clinical trials. However, auscultation and phonoangiography lack sensitivity and specificity because they are limited to diagnosing high-intensity vibrations that reach the skin surface, and the origin of the vibrations cannot be clearly resolved. Currently, there is no diagnostic tool to quantitatively image the vibrations associated with bruits at their origin. Therefore, although tissue vibrations have been shown to be important in diagnosis, their clinical use is currently limited. It would be desirable to provide non-invasive techniques for analyzing bruits and wall vibrations associated with stenosed blood vessels that are not limited to analyzing vibrations that reach the skin surface.
Advances in duplex and color-flow ultrasound in the last two decades have had a significant clinical impact on vascular diagnosis, with the simultaneous availability of anatomy and flow images in real time. Ultrasonic tissue Doppler imaging (TDI) has been used for assessment of abnormal wall motion in the cardiac wall as well as in arteries. In conventional color-flow ultrasound images, tissue vibrations from abnormal blood flow produce characteristic artifacts in the surrounding tissue. These artifacts indicate tissue vibrations and are useful for recognizing stenoses. However, they are difficult to interpret, are not quantitative and are rejected by wall filters.
With the introduction of duplex ultrasound, criteria for non-invasive assessment of stenosis severity were developed based upon flow velocity. Although these criteria have been quite useful, such techniques do not analyze the turbulence information present in the wall vibration spectra. It would be desirable to provide non-invasive ultrasound based techniques for evaluating stenosis severity that factor in wall vibrations, as well as flow velocity, to achieve enhanced diagnostic tools.
Accordingly, it would be desirable to develop new tissue vibration detection and imaging modes for ultrasound instruments in which vibrations produced by stenosed blood vessels can be detected and color-coded according to their amplitude and/or frequency. These signals could be displayed separately or overlaid on a B-mode and/or a color-flow image in real time. The tissue vibration-imaging mode might then be used for locating the origin of the vibration more precisely, relative to the patient's anatomy and/or for obtaining simultaneous information about vibrations and the underlying stenosis.